title: Cardiovascular homeostasis in hypotension associated with initial stages of severe acute pancreatitis.
abstract: OBJECTIVE
  To identify the mechanisms underlying hypotension during the early phase of severe acute pancreatitis (SAP) by analyzing whether an impaired response to vasoactive substances occurs in this pathological process.
  
  
  METHODS
  Experimental SAP was induced by infusing 5% sodium taurocholate through the main pancreatic duct in rats. Once mean arterial pressure (MAP) in animals with pancreatitis was reduced, different vasoactive substances and inhibitors were administered.
  
  
  RESULTS
  Administration of the nonspecific nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester caused a similar increase in MAP in rats with pancreatitis and control rats, whereas inducible nitric oxide synthase inhibition did not cause changes in MAP. Moreover, the hypertensive response to endothelin and angiotensin II was lower in pancreatitis. Inhibition of angiotensin II synthesis by the angiotensin-converting enzyme inhibitor perindopril in animals with pancreatitis caused severe hypotension, causing death in 40% of them. Finally, pressor hyporesponsiveness to angiotensin II in animals with pancreatitis was avoided by previous administration of perindopril and N omega-nitro-L-arginine methyl ester.
  
  
  CONCLUSIONS
  The SAP-induced hypotension is associated with a deficient pressor responsiveness to angiotensin II and endothelin-1. The renin-angiotensin system plays an important role in the control of MAP in animals with pancreatitis.
authors.affiliation: From the Department of Physiology and Pharmacology, University of Salamanca, Salamanca, Spain.
authors.forename: Mónica
authors.initials: M
authors.lastname: García
authors.forename: Ernesto
authors.initials: E
authors.lastname: Hernández-Barbáchano
authors.forename: Maria Pilar
authors.initials: MP
authors.lastname: Hernández Lorenzo
authors.forename: José Julián
authors.initials: JJ
authors.lastname: Calvo
authors.forename: José M
authors.initials: JM
authors.lastname: López Novoa
authors.forename: José Ignacio
authors.initials: JI
authors.lastname: San Román
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004195:Disease Models, Animal; D016232:Endothelins / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006706:Homeostasis; D007022:Hypotension / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D012720:Severity of Illness Index; D013656:Taurocholic Acid; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D016232:Endothelins; D004791:Enzyme Inhibitors; D000804:Angiotensin II; D013656:Taurocholic Acid; D019001:Nitric Oxide Synthase